A Breast Cancer Elf?

Breast cell transcription factor ELF5 involved in defining breast cancer subtype

/ Author:  / Reviewed by: Joseph V. Madia, MD

(RxWiki News) Here’s an intriguing thought. What if we could reprogram cancer so it responds to treatment? That’s exactly what breast cancer experts are exploring.

Someday, doctors may be able to treat breast cancer by fiddling with something called a transcription factor. Changing the levels of one transcription factor - ELF5 - may offer new therapy options.

"Ask about your latest treatment options."

This research is coming out of Australia. Christopher J. Ormandy, PhD, of The Kinghorn Cancer Centre, Garvan Institute of Medical Research, led the study that focused on ELF5.

Most breast cancers are fed by the female hormone estrogen. These are called estrogen receptor positive (ER+) cancers. Patients with this form of the disease are treated with drugs like tamoxifen and aromatase inhibitors that block estrogen.

Transcription factors are like a light switch. They turn genes on and off. ELF5 makes breast cancer cells ignore estrogen. That means estrogen-blocking drugs don’t work anymore.

ELF5 normally works in the mammary gland during pregnancy. Its role is to make the structures needed to produce milk.

In this preclinical study, researchers discovered that ELF5 can actually turn an ER+ tumor cell into an estrogen receptor negative cell. The scientists also discovered in the laboratory that ELF5 may be at the heart of why some breast cancers become difficult to treat.

"This work tells us that cancers which become refractory [no longer respond] to anti-estrogen treatment often do so by elevating their levels of ELF5 and becoming functionally estrogen receptor negative," Dr. Ormandy said in a statement. “"Our key discovery here is that by simply manipulating one transcription factor we can change the subtype of breast cancer."

Like tamoxifen, a class of drugs called aromatase inhibitors block estrogen. These drugs are: Arimidex (anastrozole), Aromasin (exemestane) and Femara (letrozole)

This research was published December 27 in PLoS Biology.

This work was funded by The National Health and Medical Research Council of Australia, New South Wales Cancer Council, Cancer Institute New South Wales, Banque Nationale de Paris-Paribas Australia and New Zealand, RT Hall Trust, Australian Cancer Research Foundation, Prostate Cancer Foundation Australia, Cure Cancer Foundation Australia, Breast Cancer Campaign UK, and the National Breast Cancer Foundation. No conflicts of interest were disclosed.

Reviewed by: 
Review Date: 
January 2, 2013
Last Updated:
January 4, 2013